They have been shown to inhibit the release of human chorionic gonadotropin (hCG) from human

placental explants, to block in vitro trophoblast migration, invasion, and multinucleated cell formation,
to inhibit trophoblast cell adhesion molecules, and to activate complement on the trophoblast surface
inducing an inflammatory response.

The antibodies generated in patients with APS appear to recognize epitopes on phospholipid-binding
proteins, unlike the antibodies that arise following infections such as syphilis and Lyme disease, which
recognize phospholipids directly.9